The proposed experiments will investigate how the circadian system regulates the expression of rapid-eye-movement (REM) sleep. This work offers new basic understanding of REM sleep physiology relevant to the clinical significance of REM sleep disturbances in depression, schizophrenia, narcolepsy, alcoholism, obsessive-compulsive disorder, and Alzheimer's disease. REM sleep has a robust circadian rhythm and appears to be homeostatically regulated in rodents and humans. Although the circadian pacemaker located in the suprachiasmatic nucleus of the hypothalamus (SCN) is thought to promote cortical and behavioral activation and oppose compensatory NREM sleep drive, it is not known how the circadian system interacts with compensatory REM sleep mechanisms. Furthermore, the essential neural connections between the SCN and the REM sleep generator in the brain-stem have not been identified. The experiments in this revised pre-doctoral NRSA proposal will investigate how circadian and homeostatic influences may be integrated to shape REM sleep by: (1) comparing the compensatory REM sleep responses of intact and SCN-lesioned rats to REM sleep deprivation at different circadian times, and (3) examining the convergence of SCN/proximal relay efferent and dorsal raphe afferent projections with FOS and glutamic acid decarboxylase (GAD67) immunohistochemistry in the vlPHA after REM sleep deprivation and compensation.